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PHAR222 > L12 Neuroendocrine Hormones > Flashcards

L12 Neuroendocrine Hormones Flashcards

1
Q

The endocrine system regulates many of the body’s activities:

A

growth; reproduction; adaption to stress; immunity; metabolic activity; glucose homeostasis; circulatory volume; Ca2+ homeostasis

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2
Q

Endocrine activities are produced by endogenous chemical messengers, called _____ which are secreted from endocrine glands.

A

endocrine hormones

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3
Q

Several major hormones are members of the neuroendocrine system, in which hormone release is regulated by the_____

A

brain

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4
Q

Parts of the endocrine system

A

The female ovaries, male testes, and pituitary, thyroid, and adrenal glands are major constituents of the endocrine system

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5
Q

Neuroendocrine anatomy

A
  • [pictures on slides] pituitary glands underneath brain. It is attached to the hypothalamus via a stalk.
  • Mainly the hypothalamus and the pituitary gland
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6
Q

Releasing factors/peptides

A

GnRH; GHRH; TRH; CRH Somatostatin (GIR)

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7
Q

Tropic hormones

A

ACTH; GH; FSH; LH; TSH; PRL

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8
Q

ACTH

A
  • Adrenocorticotropic hormone (ACTH)
  • tropic hormone produced by the A.pituitary.
  • The hypothalamic-pituitary axis controls it.
  • ACTH regulates cortisol and androgen production. (glucocorticoids and mineralcorticoids)
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9
Q

GH

A
  • growth hormone
  • growth promotion: lipids and carbohydrate metabolism
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10
Q

FSH + LH

A
  • growth of reproductive system
  • sex hormones
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11
Q

TSH

A
  • Thyroid Stimulating Hormone
  • produced by the pituitary gland.
  • regulate (stimulate) production of thyroid hormones by the thyroid gland.
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12
Q

PL

A
  • prolactin
  • milk production
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13
Q

Neuroendocrine system is diagram

A

Neural tissue
↓ RF
Endocrine system
↓ blood (tropic hormone)
Endocrine tissue/ gland
↓ blood (effector hormone). ⥀ negative feedback
Target organs/tissues
↓
Physiological response

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14
Q

Drugs (pharmacology) vs hormone

A

{slides}

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15
Q

Thyroxine hormone (gland/effect/release)

A
  • thyroid
  • Brain development; digestion; increase metabolic activity
  • TSH
  • part of hypothalamic pituitary axis
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16
Q

Insulin-like growth factor (gland/effect/release)

A
  • liver
  • Growth and metabolism
  • GH
  • hypothalamic pituitary axis
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17
Q

Cortisol (gland/effect/release)

A
  • Adrenals
  • Adaptation to stress; immunomodulation
  • ACTH
  • part of hypothalamic pituitary axis
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18
Q

Sec steroids (gland/effect/release)

A
  • Testes; ovaries; placenta
  • Reproduction; secual characteristics
  • LH, FSH
  • hypothalamic pituitary axis
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19
Q

Insulin (gland/effect/release)

A
  • pancreas
  • availability of glucose to cells
  • blood glucose levels
20
Q

Hormone release is stimulated by hypothalamic _____ ____ and pituitary trophic hormones, which regulate effector hormone_____ and actions

A

releasing factors
production

21
Q

Neuroendocrine system: example of hormone release

A

Physiologic input from the brain
↓
Hypothalamus
↓ Releasing hormone (e.g. GHRH, TRH)
↓
Pituitary gland
↓ Trophic hormone (e.g. GH, TSH)
Endocrine gland
↓ Effector hormone (e.g. IGF-1, T4)
Target organ →Effect (e.g. growth, increased metabolic rate)

22
Q

[Negative feedback control] inhibited by the endocrine hormone which exerts negative feedback effects on the____ to inhibit release of releasing and_____ hormones.

A

HPA
trophic

23
Q

Negative feedback control diagram

A

Physiologic input from the brain
↓
Hypothalamus ⬅︎ inhibit
↓. Releasing hormone
Pituitary gland ⬅︎ inhibit
↓. Trophic hormone
Endocrine gland
↓. Effector hormone ⬆︎Neg feedback
Target organ⤍Effect

24
Q

What inhibits growth hormone –> insulin-like growth factors

A

Somatostatin

25
Q

Thyrotropin releasing hormone (TRH)
↓
Thyrotropin
↓
What effector hormones

A

Thyroxine (T4 & T3)

26
Q

Hormone deficiency [hypothyroidism or type I diabetes:]

A

requires exogenous hormone replacement due to lack of endogenous production or receptor defect

27
Q

Hormone excess [e.g. acromegaly (tumour): ]

A

requires endocrine surgery or inhibitors of hormone release or action to combat excess levels

28
Q

Hormone supplementation [e.g. type II diabetes, or corticosteroid therapy for immune suppression: ]

A

exogenous hormone (or analogs) administered to amplify effect

29
Q

Hormone suppression [pituitary suppression (for IVF) or contraception: ]

A

achieved by exogenous hormones to maintain negative feedback

30
Q

Growth Hormone (GH) info (Choh Hao Li)

A
  • secretion is stimulated by GHRH & inhibited by somatostatin
  • secretion is also stimulated by deep sleep, especially in children
  • secretion is highest in the newborn and during puberty, falling dramatically with adulthood and ageing
  • 191 aa peptide, most abundant of the pituitary hormones
31
Q

Effects of GH

A
  • The major effect of GH is to stimulate normal proportional growth.
  • It does this by stimulating the production by the liver of insulin-like growth factor-1 (IGF-1)
  • IGF-1 (70 aa) stimulates protein synthesis (esp. in skeletal muscle), bone growth and cartilage synthesis
32
Q

Effects of GH diagram

A

Hypothalamus
↓ (+) ↓ (-)
GHRH Somatostatin
↓
Anterior pituitary
↓
Growth hormone (somatropin)
↓ ↓
↓ Liver
↓ ↓
↓ IGF-1
↓
Muscle, bone, etc

Feedback on slide

33
Q

______ which is identical to GH and produced by recombinant DNA technology

A

Somatropin

34
Q

Control of GH levels

A
  • Negative feedback mechanisms
    – GH inhibits GHRH release
    – IGF-1 inhibits GH release and stimulates somatostatin release
  • for tight control over GH and IGF-1 release (and actions)
  • loss of this tight control of GH production can lead to
    – lack of growth (dwarfism)
    – excess growth
    (giantism, acromegaly)
35
Q

loss of this tight control of GH production can lead to

A

– lack of growth (dwarfism)
– excess growth
(giantism, acromegaly)

36
Q

Growth Hormone Deficiency → Dwarfism

A
  • Somatropin used to achieve satisfactory growth in dwarfism caused by low GH production
  • not useful if dwarfism is caused by a lack of GH receptors - Laron dwarfism or lack of IGF-1 (African pygmies) – use human IGF-1 instead
37
Q

Normal GH

A

Anterior pituitary
↓
Growth Hormone
↓ ↓
↓ Liver
↓ ↓
↓ IGF-1
↓
Normal growth

38
Q

Hypopituitary dwarfism diagram due to pituitary gland tumor or genetic factors

A

↓ Anterior pituitary function
↓
↓ Growth Hormone
↓ ↓
↓ Liver
↓ ↓
↓ ↓ IGF-1
↓
Reduced growth

39
Q

GH excess → Giantism / Acromegaly
E.g. Pituitary gland tumor

A

↑ Anterior pituitary function
↓
↑ Growth Hormone
↓
Liver
↓
↑ IGF-1
↓
Enhanced growth

40
Q

Acromegaly

A
  • generally caused by a benign pituitary tumour and increased GH
  • enlargement mainly of the facial structures, and hands and feet
  • ↑ death rate (av. life span<10 years) due to higher rates of cardiovascular & lung disease, diabetes, etc. (not cancer)
41
Q

Overview of acromegaly treatment

A
  • Surgery → ↓tumor
  • Somatostatin Analogues → ↓GH release
  • GH- receptor antagonist → ↓GH actions
  • objective is to reduce IGF-1 levels, as elevated levels of IGF-1 are linked to higher death rates.
42
Q

Treatment of Acromegaly [surgery]

A
  • surgery = 1st line treatment (50% success rate)
    – then radiation to remove lingering tumor cells (slow response)
  • if surgery is not effective then the release of GH & IGF-1 may be inhibited by somatostatin analogues
43
Q

Treatment of Acromegaly [somatostatin analogues]

A
  • if surgery not effective then the release of GH & IGF-1 inhibited by somatostatin analogues (60-80% success rate)
  • octreotide/lanreotide (s.c. injection 2-3 times daily/ monthly)
  • pasireotide (pan SST receptor agonist, ↑ response rate)
44
Q

pasireotide

A
  • somatostatin analog
  • SST receptor agonist,
  • inhibition of ACTH secretion (not on slide)
45
Q

Treatment of Acromegaly [GH- rec antagonist]

A
  • pegvisomant GH receptor antagonist (>90% success)
46
Q

Growth hormone receptor activation

A
  • GH is a 191 amino acid protein
  • GH binds to 2 cell-surface GH receptors, resulting in receptor dimerization and activation (enzyme-linked receptor)
  • GH receptor activation –> enhanced IGF-1 expression
47
Q

GH receptor blockade (Pegvisomant)

A
  • mutant GH molecule
  • single amino acid substitution (Gly for Arg at position 120),
  • aa disrupts the binding to the 2nd GH receptor & prevents GH receptor dimerization & activation.
  • Pegvisomant (PEG) stops dimerisation → no receptor activation → No IGF-1 production

PHAR222 (25 decks)

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